Medical devices are frequently used in contact with blood in blood banks, cardiovascular applications, organ replacement and vascular surgery. These devices are made from plastics, metals or modified tissue and have in common that they activate the natural host defence mechanism of blood by a foreign body reaction (FIG. 1). One of the direct effects of blood with such a foreign surface is clotting, which is prevented by anticoagulants. The other effect is activation of the immune system, which cannot be prevented pharmacologically.
This immune response is effected by the complement system, a number of serum proteins consisting of components, activators, stabilizers and inhibitors. The complement system initiates chemotaxis and activation of leucocytes, is essential for phagocytosis of microorganisms and is capable of killing bacteria directly by inducing cell lysis. An implanted foreign body surface could also be attacked by the complement system. In view of the wide-reaching biologic effects of the complement system, the consequences of uncontrolled complement activation would be devastating (1-4). Continued activation of the sequence attracts leukocytes which release lysosomal enzymes as a byproduct of phagocytosis, which in turn cause necrosis of normal tissue (5-8).
Normally, tight controls are in effect which regulate the complement system to protect host tissue. The cascade is naturally moderated by the instability of the enzymes formed. Once a component is activated, failure to combine with its substrate within milliseconds cause it to decay. In addition, several plasma inhibitors are present to control the cascade. However, during the use of medical devices these regulatory mechanisms appear often inadequate due to the unnatural surface. Therefore, testing of complement activation by materials used for the construction of medical devices is needed to ensure the use of materials with as low complement activation as possible.